Component

Mean arterial pressure

Mean arterial pressure. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Compared to baseline, infusion of dihydrocapsaicin caused an initial increase in mean arterial blood pressure of 25% in healthy rats and 10% in resuscitated rats, and an initial tachycardic response of 30% and 20% respectively.

    Dihydrocapsaicin → Mean arterial pressure source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/20807439.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c", "start_char": 0, "end_char": 1709, "text_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c"}
    experimental_model
    Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment
    exposure
    Dihydrocapsaicin by continuous intravenous infusion at doses up to and beyond 2.0 mg/kg/h
    limitations
    The most important safety record in this collection, and the one whose population is the same population the therapy is aimed at. It is a rat study and the episodes are described rather than counted per animal.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    The first thing it does is push blood pressure and heart rate up, before anything else happens.
    primary_references
    [dhc-p20807439] Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin. (2010). https://pubmed.ncbi.nlm.nih.gov/20807439/ DOI: 10.1186/1471-2261-10-39
    tissue_or_cell_type
    Cardiovascular system

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 387–398

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment · source_derived_draft · unverified_draft

    ### dhc-initial-pressor-response Compared to baseline, infusion of dihydrocapsaicin caused an initial increase in mean arterial blood pressure of 25% in healthy rats and 10% in resuscitated rats, and an initial tachycardic response of 30% and 20% respectively. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The first thing it does is push blood pressure and heart rate up, before anything else happens. organism: Rat tissue_or_cell_type: Cardiovascular system experimental_model: Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment limitations: The most important safety record in this collection, and the one whose population is the same population the therapy is aimed at. It is a rat study and the episodes are described rather than counted per animal. exposure: Dihydrocapsaicin by continuous intravenous infusion at doses up to and beyond 2.0 mg/kg/h evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/20807439.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c", "start_char": 0, "end_char": 1709, "text_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c"} [dhc-p20807439] Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin. (2010). https://pubmed.ncbi.nlm.nih.gov/20807439/ DOI: 10.1186/1471-2261-10-39
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. At high levels of dihydrocapsaicin infusion above 2.0 mg/kg/h two single episodes of transient bradycardia and hypotension were observed in 33% of healthy rats, consistent with a TRPV1-agonist-induced Bezold-Jarisch reflex, whereas in resuscitated rats multiple episodes were observed in 100% of the rats at a dose of 0.65 mg/kg/h, and this effect could be completely blocked in the resuscitated rats by pre-treatment with the muscarinic acetylcholine antagonist atropine.

    Dihydrocapsaicin → The Bezold-Jarisch reflex of bradycardia and hypotension source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/20807439.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c", "start_char": 0, "end_char": 1709, "text_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c"}
    experimental_model
    Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment
    exposure
    Dihydrocapsaicin by continuous intravenous infusion at doses up to and beyond 2.0 mg/kg/h
    limitations
    The most important safety record in this collection, and the one whose population is the same population the therapy is aimed at. It is a rat study and the episodes are described rather than counted per animal.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    After a cardiac arrest the same drug triggers dangerous slowing of the heart at a third of the dose, and atropine stops it.
    primary_references
    [dhc-p20807439] Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin. (2010). https://pubmed.ncbi.nlm.nih.gov/20807439/ DOI: 10.1186/1471-2261-10-39
    tissue_or_cell_type
    Cardiovascular system
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 374–385

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment · source_derived_draft · unverified_draft

    ### dhc-bezold-jarisch-susceptibility At high levels of dihydrocapsaicin infusion above 2.0 mg/kg/h two single episodes of transient bradycardia and hypotension were observed in 33% of healthy rats, consistent with a TRPV1-agonist-induced Bezold-Jarisch reflex, whereas in resuscitated rats multiple episodes were observed in 100% of the rats at a dose of 0.65 mg/kg/h, and this effect could be completely blocked in the resuscitated rats by pre-treatment with the muscarinic acetylcholine antagonist atropine. Condition category: biomarker_context nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: After a cardiac arrest the same drug triggers dangerous slowing of the heart at a third of the dose, and atropine stops it. organism: Rat tissue_or_cell_type: Cardiovascular system experimental_model: Continuous intravenous infusion in healthy rats and in rats resuscitated from cardiac arrest, with atropine pre-treatment limitations: The most important safety record in this collection, and the one whose population is the same population the therapy is aimed at. It is a rat study and the episodes are described rather than counted per animal. exposure: Dihydrocapsaicin by continuous intravenous infusion at doses up to and beyond 2.0 mg/kg/h evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/20807439.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c", "start_char": 0, "end_char": 1709, "text_sha256": "49bfe9de2b31cccc9afa70d322f9c96256968e48fdc033102fdb46394e617b0c"} [dhc-p20807439] Increased susceptibility to cardiovascular effects of dihydrocapcaicin in resuscitated rats. Cardiovascular effects of dihydrocapsaicin. (2010). https://pubmed.ncbi.nlm.nih.gov/20807439/ DOI: 10.1186/1471-2261-10-39
    Complete structured claim and evidence

  2. Dihydrocapsaicin at 1.25 mg/kg produced a stable drop in core temperature to 33 degrees in naive and ischaemia-reperfusion mice but not in TRPV1 knockout mice, and had no measurable effect on heart rate or cerebral perfusion while producing a slight transient drop in mean arterial pressure of less than 6 millimetres of mercury.

    Dihydrocapsaicin → Hypothermia induced by a drug rather than by physical cooling source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"}
    experimental_model
    Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion
    exposure
    Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm
    limitations
    The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Mouse
    plain_language
    The cooling happens through the receptor, and in these mice it barely touched the circulation.
    primary_references
    [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    tissue_or_cell_type
    Brain and cardiovascular system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 296–307

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion · source_derived_draft · unverified_draft

    ### dhc-hypothermia-requires-trpv1 Dihydrocapsaicin at 1.25 mg/kg produced a stable drop in core temperature to 33 degrees in naive and ischaemia-reperfusion mice but not in TRPV1 knockout mice, and had no measurable effect on heart rate or cerebral perfusion while producing a slight transient drop in mean arterial pressure of less than 6 millimetres of mercury. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The cooling happens through the receptor, and in these mice it barely touched the circulation. organism: Mouse tissue_or_cell_type: Brain and cardiovascular system experimental_model: Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion limitations: The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects. exposure: Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"} [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    Complete structured claim and evidence

  3. Comparing bolus injection with femoral vein infusion, cardiovascular effects were seen only with a large-dose dihydrocapsaicin bolus injection, and four-hour infusion at 0.75 mg/kg/h after cardiac arrest maintained a body temperature of about 34 degrees for at least eight hours with treated rats remaining viable, showing higher electrical activity during the first four hours and better neurological recovery over three days than normothermia rats.

    Dihydrocapsaicin → Heart rate source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/28268688.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90c0491fa4681d112ecfc224671b763a608eeb03af4bf563955dc49ef628b851", "start_char": 0, "end_char": 1500, "text_sha256": "90c0491fa4681d112ecfc224671b763a608eeb03af4bf563955dc49ef628b851"}
    experimental_model
    Asphyxial cardiac arrest in rats comparing bolus injection with femoral vein infusion
    exposure
    Dihydrocapsaicin by bolus injection or by infusion at 0.75 mg/kg/h for four hours after cardiac arrest
    limitations
    Directly compares two routes of the same drug and finds the route decides whether the cardiovascular effects appear. Neurological recovery was followed for only three days.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    Injected all at once it disturbs the heart; infused slowly it does not, and the animals did better.
    primary_references
    [dhc-p28268688] Dihydrocapsaicin-induced hypothermia after asphyxiai cardiac arrest in rats. (2016). https://pubmed.ncbi.nlm.nih.gov/28268688/ DOI: 10.1109/embc.2016.7591082
    tissue_or_cell_type
    Brain and cardiovascular system

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 361–372

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Asphyxial cardiac arrest in rats comparing bolus injection with femoral vein infusion · source_derived_draft · unverified_draft

    ### dhc-route-decides-safety Comparing bolus injection with femoral vein infusion, cardiovascular effects were seen only with a large-dose dihydrocapsaicin bolus injection, and four-hour infusion at 0.75 mg/kg/h after cardiac arrest maintained a body temperature of about 34 degrees for at least eight hours with treated rats remaining viable, showing higher electrical activity during the first four hours and better neurological recovery over three days than normothermia rats. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Injected all at once it disturbs the heart; infused slowly it does not, and the animals did better. organism: Rat tissue_or_cell_type: Brain and cardiovascular system experimental_model: Asphyxial cardiac arrest in rats comparing bolus injection with femoral vein infusion limitations: Directly compares two routes of the same drug and finds the route decides whether the cardiovascular effects appear. Neurological recovery was followed for only three days. exposure: Dihydrocapsaicin by bolus injection or by infusion at 0.75 mg/kg/h for four hours after cardiac arrest evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/28268688.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90c0491fa4681d112ecfc224671b763a608eeb03af4bf563955dc49ef628b851", "start_char": 0, "end_char": 1500, "text_sha256": "90c0491fa4681d112ecfc224671b763a608eeb03af4bf563955dc49ef628b851"} [dhc-p28268688] Dihydrocapsaicin-induced hypothermia after asphyxiai cardiac arrest in rats. (2016). https://pubmed.ncbi.nlm.nih.gov/28268688/ DOI: 10.1109/embc.2016.7591082
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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